Host adaptation

When considering pathogens, host adaptation can have varying descriptions. For example, in the case of Salmonella, host adaptation is used to describe the "ability of a pathogen to circulate and cause disease in a particular host population." Another usage of host adaptation, still considering the case of Salmonella, refers to the evolution of a pathogen such that it can infect, cause disease, and circulate in another host species. While there might be pathogens that can infect other hosts and cause disease, the inability to pervade, or spread, throughout the infected host species indicates that the pathogen is not adapted to that host species. In this case, the ability or lack thereof of a pathogen to adapt to its host environment is an indicator of the pathogen's fitness or virulence. If a pathogen has high fitness in the host environment, or is virulent, it will be able to grow and spread quickly within its host. Conversely, if the pathogen is not well adapted to its host environment, then it will not spread or infect the way a well adapted pathogen would.

Pathogens like Salmonella, which is a food borne pathogen, are able to adapt to the host environment and maintain virulence via several pathways. In a paper by Baumler et al 1998, characters of Salmonella, such as its ability to cause intestinal infection were attributed to virulence factors like its ability to invade intestinal epithelial cells, induce neutrophil recruitment and interfere with the secretion of intestinal fluid. Phylogenetic analysis also revealed that many strains or lineages of Salmonella exist, which is advantageous for the pathogen because its genetic diversity can acts as fodder for natural selection to tinder with. For instance, if a particular Salmonella strain is more fit in the host stomach environment, compared to other Salmonella strains, then the former will be positively selected for and increase in prevalence. Eventually this strain will colonize and infect the stomach. The other less fit strains will be selected against and will thus not persist. Another major host adaptation on the part of Salmonella was its adaptation to host blood temperatures. Because Salmonella can thrive at the human host temperature, 98.6 degrees F, it is fit for the host environment and hence survive well in it. Adaptations like these are simple yet very effective ways of infecting hosts because they use the host's body and important feature of its body as a stepping stone in the infection process.

Another intestinal pathogen in the genus Cryptosporidium, which was not always a human pathogen, "recently" adapted to the human host environment. Numerous phylogenetic analyses in a paper by Xiao et al 2002 indicated that the Cryptosporidium parvum bovine genotype and Cryptosporidium meleagridis were originally parasites of rodents and mammals, respectively. However, this parasite 'recently' expanded into humans. As was previously mentioned, the ability to survive in different host species is an adaptation that is highly advantageous to pathogens because it increases their chances for survival and circulation. Some pathogens can evolve to become resistant to the body's natural immune defenses and/or to outside intervention like drugs. For instance, Clostridium difficile is the most frequent cause of nosocomial diarrhea worldwide, and reports in the early 2000s indicated the advent of a hypervirulent strain in North America and Europe. In study by Stabler et al 2006, comparative phylogenomics (whole-genome comparisons using DNA microarrays combined with Bayesian phylogenies) were used to model the phylogeny of C. difficile. Phylogenetic analysis identified four distinct statistically significant 'clusters' making a hypervirulent clade, a toxin A− B+ clade, and two clades with human and animal isolates. Genetic differences between the four groups revealed significant findings related to virulence. The authors saw that hypervirulent strains had undergone various types of niche adaptation like antibiotic resistance, motility, adhesion, and enteric metabolism.

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